The major objective of this research is to define the mechanism by which 1,25(OH)2D3 alters transcellular calcium transport in the small intestine of the chick. Previous work has identified the luminal membrane as a major site of action of this hormone. At this site, the hormone increases the rate of entry of calcium into the cell. Using a method developed in this laboratory, we have studied the rate of calcium uptake into membrane vesicles prepared from D-deficient and 1,25(OH)2D3-treated chicks. Treatment with 1,25(OH)2D3 leads to an increase in the rate of calcium uptake into these vesicles. The present proposal is to explore the possibility that the major action of the hormone is upon the lipid structure of the membrane, and that this structural change is responsible for mediating the change in calcium transport. The hypothesis is to be tested by: 1) examining the effect of 1,25(OH)2D3 on phospholipid metabolism; 2) exploring the effect of artifically-induced changes in membrane fluidity upon calcium transport; 3) carrying out lipid protein exchanges between the two types of membranes; and 4) examining the effect of 1,25(OH)2D3 a on lipid turnover in other possible target membranes; and 4) examining the effect of 1,25(OH)2D3 on lipid turnover in other possible target membranes. A study of the relationship between lipid turnover ans 1,25(OH)2D3-regulated phosphate transport in membrane vesicles will also be undertaken.